Dr. Qiang’s laboratory focuses on the Wnt signaling pathway in the pathogenesis of myeloma and identification of molecular targets for myeloma cells that are resistant to chemotherapy. The laboratory has characterized that Wnt signaling is activated in myeloma cells in order to regulate migration and invasion of myeloma cells. Disruption of Wnt signaling by myeloma-derived Dkk1 is an important mechanism underlying myeloma-triggered bone disease. In the bone marrow, Dkk1 suppresses the Wnt pathway. This leads directly to diminished differentiation of mesenchymal stem cells into osteoblasts and indirectly promotes osteoclast activity via de-regulation of RANK/OPG by osteoblasts in the bone marrow. Discoveries in Dr. Qiang’s laboratory have also generated mechanistic insight into how proteasome inhibitors act against bone disease by promoting differentiation of mesenchymal stromal cells via Wnt-independent activation of the beta-catenin-TCF pathway.

Dr. Qiang’s team is working to identify molecular targets in the tumor microenvironment that harbors myeloma cells that are resistant to chemotherapy. They are also investigating the role of the MAF family in the development and progression of myeloma. They are elucidating the molecular mechanisms underlying the protection of MAF protein from degradation and are identifying molecular targets that are regulated by MAF in order to develop novel therapies.